ArticleArthritis & rheumatology (Hoboken, N.J.)2025
FoxO1 Deficiency in Monocytic Myeloid-Derived Suppressor Cells Exacerbates B Cell Dysfunction in Systemic Lupus Erythematosus.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Epigenetic regulation of B cell tolerance and dysfunction in autoimmune disease.Nature reviews. Immunology · 2026Review
- Effects and molecular mechanism of inhibiting p53 signaling pathway by NSUN4 on the resistance to BCL-2 inhibitor for diffuse large B-cell lymphoma.Clinical and experimental medicine · 2026Article
- Inference of marker genes of subtle cell state changes via iLR: iterative logistic regression.Bioinformatics (Oxford, England) · 2026Article
- The multiple roles of Ggt1-Cre in the generation of transgenic mice.Cellular & molecular biology letters · 2026Article
- Astragalosides Promote MH7A Cell Apoptosis by Suppressing WTAP-mediated m6A Methylation of TRAIL-DR4.Combinatorial chemistry & high throughput screening · 2026Article
- Myeloid-Derived Suppressor Cells: Immunoregulatory Roles and Therapeutic Prospects in Immune-Mediated Hematological Disorders.Journal of immunology research · 2026Review
- Epitranscriptomic regulation by m6A in immunity and autoimmune disorders: emerging mechanisms and clinical perspectives.Frontiers in immunology · 2026Review
- RNA methylation in autoimmune rheumatic diseases: mechanisms and therapeutic potential.Frontiers in immunology · 2026Review
- Epigenetic modifier m⁶A methylation: insights into the pathogenesis and therapeutic potential of autoimmune diseases.Journal of translational medicine · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
objectiveMyeloid-derived suppressor cells (MDSCs) contribute to the pathogenesis of systemic lupus erythematosus (SLE), in part due to promoting the survival of plasma cells. FoxO1 expression in monocytic MDSCs (M-MDSCs) exhibits a negative correlation with the SLE Disease Activity Index score. This study aimed to investigate the hypothesis that M-MDSC-specific FoxO1 deficiency enhances aberrant B cell function in aggressive SLE.
methodsWe used GEO data sets and clinical cohorts to verify the clinical significance of FoxO1 expression and circulating M-MDSCs. Using Cre-LoxP technology, we generated myeloid FoxO1 deficiency mice (mFoxO1
resultsWe present evidence that low FoxO1 is predominantly expressed in M-MDSCs in both patients with SLE and lupus mice, and mice with myeloid FoxO1 deficiency (mFoxO1
conclusionOur findings indicate that effective inhibition of B cells mediated by the ALKBH5/FoxO1/Met axis in M-MDSCs could offer a novel therapeutic approach to manage SLE.
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